Tyrosine hydroxylase expression in chronically stressed postpartum rats

Lecture Centre Concourse

Postpartum depression (PPD) is a common mental health disorder associated with maternal suffering and negative consequences for offspring, affecting 1 in 7 women. PPD shares similar symptoms as major depressive disorder. However, the causes of postpartum depression (PPD) are incompletely understood but include social influences and biological mechanisms. The postpartum period is characterized by dramatic hormone fluctuations and represents a time of increased risk for developing depression. Stress and the early cessation of breastfeeding (or lack thereof) are major risk factors for PPD. Hormonal aspects of breastfeeding may buffer against the development of PPD. Prolactin, a hormone elevated during lactation, attenuates stress responses in postpartum rats. The dopaminergic system is particularly important in understanding PPD. Anhedonia, loss of pleasure in previously rewarding stimuli, is a core symptom of depression and may be related to disturbances in the dopamine (DA) system. Tyrosine hydroxylase (TH) is the enzyme that makes DA and TH can be used to identify DA neurons. In this study we tested whether chronic stress would reduce TH-expressing neurons in the ventral tegmental area (VTA) and whether prolactin would reverse this. Rats were randomly assigned to be chronically stressed or non-stressed and treated daily with prolactin or saline. Using immunohistochemistry, we have labeled for TH and are currently conducting microscopy. Utilizing an interdisciplinary biopsychosocial approach that includes perspectives in neuroscience and social work will enhance treatment of PPD and improve the overall quality of life for women who are afflicted.